Research progress on the role and mechanism of ferroptosis in heart diseases.
- Author:
Yu-Tong CUI
1
;
Xin-Xin ZHU
1
;
Qi ZHANG
1
;
Ai-Juan QU
1
Author Information
1. Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China.
- Publication Type:English Abstract
- MeSH:
Ferroptosis/physiology*;
Humans;
Heart Diseases/physiopathology*;
NF-E2-Related Factor 2/physiology*;
Animals;
Myocardial Reperfusion Injury/physiopathology*;
Lipid Peroxidation;
Heart Failure/physiopathology*;
Iron/metabolism*;
Diabetic Cardiomyopathies/physiopathology*;
Ubiquinone/analogs & derivatives*
- From:
Acta Physiologica Sinica
2025;77(1):75-84
- CountryChina
- Language:Chinese
-
Abstract:
Cardiovascular disease remains the leading cause of death in China, with its morbidity and mortality continue to rise. Ferroptosis, a unique form of iron-dependent cell death, plays a major role in many heart diseases. The classical mechanisms of ferroptosis include iron metabolism disorder, oxidative antioxidant imbalance and lipid peroxidation. Recent studies have found many additional mechanisms of ferroptosis, such as coenzyme Q10, ferritinophagy, lipid autophagy, mitochondrial metabolism disorder, and the regulation by nuclear factor erythroid 2-related factor 2 (NRF2). This article reviews recent advances in understanding the mechanisms of ferroptosis and its role in heart failure, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, myocardial toxicity of doxorubicin, septic cardiomyopathy, and arrhythmia. Furthermore, we discuss the potential of ferroptosis inhibitors/inducers as therapeutic targets for heart diseases, suggesting that ferroptosis may be an important intervention target of heart diseases.
